A case report of undiagnosed postpartum hemolytic uremic syndrome.

BACKGROUND: Postpartum hemolytic uremic syndrome (PHUS) is a severe thrombotic microangiopathy (TMA) that is clinically characterized by hemolytic anemia, renal dysfunction, and low platelet levels after childbirth. Here, we report a rare case of unexpected death due to PHUS. CASE PRESENTATION: A 23-year-old parturient had an uncomplicated cesarean section at 40 weeks gestation. The immediate postpartum course was uneventful. However, eight days post delivery, the patient developed severe nausea and vomiting followed by hematuria, spontaneous bruising, marked pallor, icteric sclera, and lethargy. Laboratory findings revealed that the patient had hemolytic anemia, thrombocytopenia, and acute renal failure. This patient died approximately 29 h after the onset of symptoms. Post-mortem examination confirmed that the patient had PHUS. CONCLUSIONS: This paper addresses the need for a renal histological examination in addition to a thorough clinical history and appropriate laboratory tests for the rapid and accurate diagnosis of PHUS. Early detection and diagnosis can significantly improve the prognosis and optimize maternal outcomes.

Sudden death in custody due to pituitary apoplexy during long restriction in a sitting position: a case report and review of the literature.

Pituitary apoplexy is an uncommon clinical emergency arising from hemorrhage into or infarction of a pituitary adenoma. The most common presentation is sudden headache, visual field defects and signs of hypopituitarism. It usually occurs in the age group from 20 to 50 years and affects more male than female. Sudden death due to pituitary apoplexy without common symptoms is rarely reported. Here, we described a scarcely-reported case of sudden death in custody caused by pituitary apoplexy resulting from stress-induced hemorrhage of gonadotroph adenoma, a kind of pituitary adenoma, without common clinical symptoms. In this case, a 49-year-old man was restrained in a sitting position for 4 days and died unexpectedly. At autopsy, external examination showed free of trauma. Destruction of bony structure and a circumscribed pituitary tumor were observed in sella turcica. Immunohistochemically, the tumor cells were particular positive for follicle-stimulating hormone (FSH) and luteinizing hormone (LH), thus clarifying the presence of a pituitary gonadotroph adenoma. We provide the case description and a short review of pituitary apoplexy and pituitary adenoma as a rare cause of sudden death.

Sudden death due to lupus-induced pancarditis diagnosed after necropsy: a case report.

Systemic lupus erythematosus (SLE) is an autoimmune connective tissue disease affecting many organs and which is predominant in females. Although various manifestations of SLE may result in sudden death, pancarditis is very rarely encountered in forensic practice. We report on a case of sudden death caused by lupus-induced pancarditis. A 24-year-old male had pneumonia and intractable fever as initial signs when he was admitted to hospital. The patient had no symptoms associated with the cardiovascular system up to 3 days before he died. The echocardiogram and electrocardiogram were normal and diagnosis was not made until necropsy. This case is reported to broaden our understanding about the complexity of manifestations associated with SLE and inform clinicians and medical examiners of the potential for this type of lupus-induced pancarditis.

Role of neuropeptide Y and peroxisome proliferator-activated receptor γ coactivator-1α in stress cardiomyopathy / 华中科技大学学报（医学）（英德文版）

Death following situations of intense emotional stress has been linked to the cardiac pathology described as stress cardiomyopathy, whose pathomechanism is still not clear. In this study, we sought to determine, via an animal model, whether the transcriptional coactivator peroxisome proliferator-activated receptor γ coactivator-1alpha (PGC-1α) and the amino peptide neuropeptide Y (NPY) play a role in the pathogenesis of this cardiac entity. Male Sprague-Dawley rats in the experimental group were subjected to immobilization in a plexy glass box for 1 h, which was followed by low voltage electric foot shock for about 1 h at 10 s intervals in a cage fitted with metallic rods. After 25 days the rats were sacrificed and sections of their hearts were processed. Hematoxylin-eosin staining of cardiac tissues revealed the characteristic cardiac lesions of stress cardiomyopathy such as contraction band necrosis, inflammatory cell infiltration and fibrosis. The semi-quantitative RT-PCR analysis for PGC-1α mRNA expression showed significant overexpression of PGC1-α in the stress-subjected rats (P<0.05). Fluorescence immunohistochemistry revealed a higher production of NPY in the stress-subjected rats as compared to the control rats (P=0.0027). Thus, we are led to conclude that following periods of intense stress, an increased expression of PGC1-α in the heart and an overflow of NPY may lead to stress cardiomyopathy and even death in susceptible victims. Moreover, these markers can be used to identify stress cardiomyopathy as the cause of sudden death in specific cases.

Role of neuropeptide Y and peroxisome proliferator-activated receptor γ coactivator-1α in stress cardiomyopathy / 华中科技大学学报（医学）（英德文版）

Death following situations of intense emotional stress has been linked to the cardiac pathology described as stress cardiomyopathy, whose pathomechanism is still not clear. In this study, we sought to determine, via an animal model, whether the transcriptional coactivator peroxisome proliferator-activated receptor γ coactivator-1alpha (PGC-1α) and the amino peptide neuropeptide Y (NPY) play a role in the pathogenesis of this cardiac entity. Male Sprague-Dawley rats in the experimental group were subjected to immobilization in a plexy glass box for 1 h, which was followed by low voltage electric foot shock for about 1 h at 10 s intervals in a cage fitted with metallic rods. After 25 days the rats were sacrificed and sections of their hearts were processed. Hematoxylin-eosin staining of cardiac tissues revealed the characteristic cardiac lesions of stress cardiomyopathy such as contraction band necrosis, inflammatory cell infiltration and fibrosis. The semi-quantitative RT-PCR analysis for PGC-1α mRNA expression showed significant overexpression of PGC1-α in the stress-subjected rats (P<0.05). Fluorescence immunohistochemistry revealed a higher production of NPY in the stress-subjected rats as compared to the control rats (P=0.0027). Thus, we are led to conclude that following periods of intense stress, an increased expression of PGC1-α in the heart and an overflow of NPY may lead to stress cardiomyopathy and even death in susceptible victims. Moreover, these markers can be used to identify stress cardiomyopathy as the cause of sudden death in specific cases.

Seven cases of fatal aconite poisoning: forensic experience in China.

This paper presents seven fatal cases of aconite poisoning encountered in the Tongji Center for Medicolegal Expertise in Hubei (TCMEH), China, from 1999 to 2008 retrospectively. In six of the cases, deaths occurred after drinking homemade medicated liquor containing aconite, and in one case death was due to ingestion of traditional Chinese medication containing aconite. Forensic autopsy and pathological examinations ruled out the presence of physical trauma or life-threatening diseases. Diagnosis of aconite poisoning was made after postmortem toxicological analysis. Animal experiment was performed in one case demonstrating that the medicated liquor could cause death rapidly. We present the autopsy and histopathological findings, toxicological analysis, and results of animal experiment done on samples from those seven cases. As an important herbal Chinese medicine, Aconitum species deserve special attention, especially because it contains poisonous alkaloids.

Unexpected death of a young woman: is myocardial bridging significant?--A case report and review of literature.

Myocardial bridging (MB) refers to a congenital condition where a segment of a major coronary artery courses within the myocardium for a variable distance, and has been reported as an incidental finding in many cases. However, in some situations it has been shown to be associated with acute coronary syndromes, arrhythmias, myocardial ischemia and sudden death. We present the case of a 26-year-old Chinese woman with no previous history of disease who died unexpectedly in hospital. She had a 'common cold' with its associated symptoms. Autopsy revealed the presence of MB of the left anterior descending artery and microscopic examination showed associated cardiac lesions such as contraction band necrosis and interstitial fibrosis in the region supplied by the embedded artery. The coronaries were otherwise patent. Gross and microscopic examination of other organs was unremarkable. Toxicological analysis of body fluids and stomach content excluded death due to either drug intoxication or known poisonous substances. MB could have been responsible for death, but the disparate attitudes towards this phenomenon made this assumption open to discussion. We provide the case description and a short review of the literature on fatal and near- fatal cases involving MB.

Role of reactive oxygen species in triptolide-induced apoptosis of renal tubular cells and renal injury in rats / 华中科技大学学报（医学）（英德文版）

This study investigated the role of reactive oxygen species (ROS) in the pathogenesis of triptolide-induced renal injury in vivo. Rats were randomly divided into 4 groups (n=5 in each): triptolide group in which the rats were intraperitoneally injected with triptolide solution at a dose of 1 mg/kg of body weight on day 8; control group in which the rats received a single intraperitoneal injection of 0.9% physiological saline on day 8; vitamin C group in which the rats were pretreated with vitamin C by gavage at a dose of 250 mg/kg of body weight per day for 7 days before the same treatment as the control group on day 8; triptolide+vitamin C group in which the rats were first subjected to an oral administration of vitamin C at a dose of 250 mg/kg of body weight per day for 7 days, and then to the same treatment as the triptolide group on day 8. All the rats were sacrificed on day 10. Blood samples were collected for detection of plasma creatinine (Pcr) and plasma urea nitrogen (PUN) concentrations. Both kidneys were removed. The histological changes were measured by haematoxylin-eosin (HE) staining. The production of ROS was determined by detecting the fluorescent intensity of the oxidation-sensitive probe rhodamine 123 in renal tissue. Renal malondialdehyde (MDA) content was measured to evaluate lipid peroxidation level in renal tissue. TUNEL staining was performed to assess apoptosis of renal tubular cells. Renal expression of apoptosis-related proteins Bcl-2, Bax, Bid, Bad, Fas and FasL, as well as corresponding encoding genes were assessed by Western Blotting and real-time PCR. The results showed that triptolide treatment promoted the generation of a great amount of ROS, up-regulated the expression of Bax, Bid, Bad, Fas and FasL at both protein and mRNA levels, as well as the ratio of Bax to Bcl-2, and caused the apoptosis of renal tubular cells and renal injury. However, pretreatment with an antioxidant, vitamin C, significantly reduced the generation of ROS and effectively inhibited the triptolide-induced apoptosis of renal tubular cells and renal injury. It was concluded that ROS plays a critical role in triptolide-induced apoptosis of renal tubular cells and renal injury. The protective administration of vitamin C may help alleviate triptolide-induced renal injury and nephrotoxicity.

Characterization of protein in old myocardial infarction by FTIR micro-spectroscopy.

The aim of the present study was to assess whether Fourier transform infrared spectrometry (FTIR) micro-spectroscopy could produce distinct spectral information on protein of old myocardial infarction (OMI) and to set them as molecular markers to diagnose atypical OMI. Paraffin-embedded heart samples were derived from victims dying of OMI. In combination with histological stain, FTIR and infrared micro-spectroscopy, the characteristics of OMI were analyzed morphologically and molecularly. The most relevant bands identified were the amide A, B, I and, II showing crucial spectral differences between apparent normal region and OMI region, including the peak position blue shift and the increased intensity of OMI, moreover relative increase in alpha-helix and decrease in beta-sheet of protein secondary structures in OMI. Comparing to single spectral band, the I1650/I1550 ratio was increased and rationally used as a molecular marker for diagnosing OMI. These novel preliminary findings supported further exploration of FTIR molecular profiling in clinical or forensic study, and were in accordance with histopathology.

Characterization of Protein in Old Myocardial Infarction by FTIR Micro-spectroscopy / 华中科技大学学报（医学）（英德文版）

The aim of the present study was to assess whether Fourier transform infrared spectrometry (FTIR)micro-spectroscopy could produce distinct spectral information on protein of old myocardial infarction(OMI)and to set them as molecular markers to diagnose atypical OMI.Paraffin-embedded heart samples were derived from victims dying of OMI.In combination with histological stain,FTIR and infrared micro-spectroscopy,the characteristics of OMI were analyzed morphologicallyand molecularly.The most relevant bands identified were the amide A,B,Ⅰ and Ⅱ,showing crucial spectral differences between apparent normal region and OMI region,including the peak position blue shift and the increased intensity of OMI,moreover relative increase in a-helix and decrease in β-sheet of protein secondary structures in OMI.Comparing to single spectral band,the I1650/I1550 ratio was increased and rationally used as a molecular marker for diagnosing OMI.These novel preliminary findings supported further exploration of FTIR molecular profiling in clinical or forensic study,and were in accordance with histopathology.

[Noncompaction of ventricular myocardium and its medicolegal evaluation].

Noncompaction of ventricular myocardium (NVM) is a rare cardiomyopathy. For the past few years, there have been more clinical reports and related scientific researches on NVM. It is one of the hottest topics in the field of clinical cardiovascular science. NVM is rare, but usually leads to fatal results, such as sudden unexpected death. Most forensic medical examiners in China have not recognized the importance of this disease. There are no good forensic pathological methods yet to identify this disease. Furthermore, NVM is easily to be confused with other types of heart diseases. As a result, we should be very careful about NVM, and understand the importance of making right diagnosis of NVM. This review focuses on NVM's pathological features, clinical diagnostic methods, and differential diagnosis from other cardiac disease. The key points on how to make right forensic pathological diagnosis of NVM have also been summarized.